Lipids – Part 2

McCafferty

LIPID DIGESTION & ABSORPTION

Absorbable forms:

Remember “hydrolysis?”

MouthMechanical: chewing, mixed w/saliva for lubrication

Chemical:

Stomach

Mechanical: peristalsis/churning

____________

Chemical:

For digestion to continue, these fat droplets must be emulsifiedSmall IntestineFat droplets enter small intestinegallbladder contracts and releases __________

synthesized in the ______,

stored in the __________

made from _________

Once fat is emulsified into the liquid, enzymes can work:

Pancreas releases: pancreatic lipase

TG _________________________________(DRAW BELOW:)

Lipid AbsorptionSmall lipid fragments:

Glycerol and Short Chain FAs (SCFAs)Absorbed directly into the bloodstream Portal vein to liver

Lipid AbsorptionBig lipid fragments

Monoglycerides and LCFAs need help! If absorbed into the blood:

They need to be emulsified.

Big lipid fragments, cont.

Enter intestinal cell, re-form TGTG is incorporated into Lipoprotein carriers: Chylomicrons (CM)

Lipoprotein = lipid associated w/proteins

“Shuttle”

Protein and phospholipid act as emulsifiers for the other lipids

Lymph vessel

The tissues can extract what they need from the CMs.

CM remnants

Lipoproteins -- OverviewLipids bound to protein

Spherical structure – “Shuttle”

Classes of LipoproteinsWhat is denser, lipid or protein?

CM chylomicron –

made in intestinal cells

Transports ________TG from ________ to tissues

eg. adipose and muscle

VLDL – very low density lipoprotein

made in liver

Carries TG to tissues

LDL – Made in liverCarries

HDL – Made in liver & intestine

Associated w/ risk for CVD

Recommended LevelsTotal cholesterol

For 30 yrs For 30 yrs (for kids 170 mg/dl)

LDL cholesterol HDL cholesterol Triglycerides (TG) *note controversy surrounding these numbers

LDL to HDL ratioMen: Women:

LDL cholesterol increases with

HDL cholesterol increases with

STORAGE & USE OF FATOverview:

TG is main form of stored E in the bodyAdipose – When body needs fuel

Storing Fat

TG in blood (in CMs and VLDL)(need to get TG into adipose & muscle cells)

INSULIN presentActivates enzyme on blood vessel wall:LPL Lipoprotein LipaseLPL binds w/CM or VLDL and extracts TGBreaks down TG glycerol & 3FAs enter cell

Storing FatIn adipose, TG fat droplets

Storing Fat

In adipose, TG

Adipose cells stretch to hold fat

Once filled to max capacity, cells begin to multiply

Mobilizing Stored Fat

TG in adipose; want to release FAs for E

Activates enzyme inside adipose cellHSL Hormone-sensitive lipase HSL breaks down TG G & FAs

FAs blood Hydrophobic, so bound to protein carrier: albumin cells metabolized for E

USING FAT TO MAKE ATP

•What kind of fat gets used for energy?•What is triglyceride made of?

______________

_____________

_____________

Krebs

ETS

ATP

C-C-C

C-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C C-C C-CC-C

Glycerol is converted to pyruvate

can either glucose or acetyl CoA /Krebs/ATP

Fatty Acids (too large to enter Krebs cycle)

can ONLY enter energy metabolism at

Therefore,

So what’s the point?

If we are out of glycogen and need to make glucose for those glucose-dependent tissues, we aren’t going to be able to use fatty acids to do it.

Summary of ATP Production From Fat

Fat is comprised mainly of TG moleculesGlycerol and 3 FAs

Glycerol (3C) enters energy metabolism at pyruvateFAs (broken down to 2C units) enter at acetyl CoAFat can provide a very small amount of glucose form the glycerolComplete oxidation of TG yields ATP, CO2, H2O and body heat.

Cardiovascular Disease

Cardiovascular Disease – general term for diseases of the heart and blood vessels

Coronary Heart Disease (CHD) – AKA Coronary Artery Disease– lack of blood flow to the network of blood vessels surrounding (and serving) the heart.

major cause: atherosclerosis.Atherosclerosis – thickening and hardening of the walls of the blood vessels 2 deposits of fatty material (plaque)

esp. coronary and carotid arteries and abdominal aorta

Heart Attack – Lack of blood flow to the heart muscle resulting in tissue damage and sometimes sudden death

Stroke –blood flow to a part of the brain is cut off

“brain attack.” Usually due to atherosclerosis in the carotid arteries.

Atherosclerosis

Slow, progressive disease which begins in childhood and takes decades to advance.

Coronary arteries are most often affected.

“Response to Injury Theory”Fatty streaks form along arterial wallsProliferation of smooth muscle cells, WBCs and calcium plaques Plaques cause the arteries to lose

elasticity

Thrombosis:

Embolism:

Angina: pain, pressure, and tightness in chest,

back, neck, and arms caused by

Hypertension

The FOUR major risk factors:1. Smoking

HDL, BP, increases platelet stickiness (clots)

2. Hypertension cardiac work, arterial damageRisk :

3. Elevated blood cholesterol major lipid in plaque

4. Lack of regular exercise Sedentary people (60% of US) have double the risk of developing CVD as active people.

Other risk factors include:Heredity – parent or sibling male under 55, woman under 65Gender – male

women post menopause without estrogen

Age Stress and personality type

Type “A” personality, stress, depression

Elevated triglyceridesInversely correlated w/HDL’s

HomocysteineStrong + correlation w/premature diseasewith inadequate B vitamins

(folate, B6 and B12 – fruits and veggies, lean meats)

Also:

ExerciseStrengthens heart muscleLower body fat (also affects diabetes)Better glucose control blood pressure stressExercisers are less likely to be smokersImproved lipid profile (LDL, HDL) blood clotting

Dietary Prevention of Heart Disease

Fat

Saturated fat

Mono vs. Poly

Trans FAs

Sodium

Alcohol

Antioxidants and Phytochemicals

Fiber

Fish

Soy